Lipids convey both structural and functional properties to eukaryotic membranes. Understanding the basic lipid composition and the dynamics of these important molecules, in the context of cellular membranes, can shed light on signaling, metabolism, trafficking, and even membrane identity. The development of genetically encoded lipid biosensors has allowed for the visualization of specific lipids inside individual, living cells. However, a number of caveats and considerations have emerged with the overexpression of these biosensors. In this Technical Perspective, we provide a current list of available genetically encoded lipid biosensors, together with criteria that determine their veracity. We also provide some suggestions for the optimal utilization of these biosensors when both designing experiments and interpreting results.
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http://dx.doi.org/10.1091/mbc.E17-12-0738 | DOI Listing |
Mol Cancer Res
January 2025
Fox Chase Cancer Center, Philadelphia, PA, United States.
Breast cancers of the IntClust-2 type, characterized by amplification of a small portion of chromosome 11, have a median survival of only five years. Several cancer-relevant genes occupy this portion of chromosome 11, and it is thought that overexpression of a combination of driver genes in this region is responsible for the poor outcome of women in this group. In this study we used a gene editing method to knock out, one by one, each of 198 genes that are located within the amplified region of chromosome 11 and determined how much each of these genes contributed to the survival of breast cancer cells.
View Article and Find Full Text PDFPlant Mol Biol
January 2025
Department of Agricultural and Environmental Sciences, University of Milan, via Celoria 2, 20133, Milan, Italy.
OsMAIL1 encodes for a rice protein of the Plant Mobile Domain (PMD) family and is strongly upregulated during floral induction in response to the presence of the florigens Heading date 3a (Hd3a) and RICE FLOWERING LOCUS T1 (RFT1). Although OsMAIL1 expression depends on the florigens, osmail1 null mutants do not show delay in flowering time, rather OsMAIL1 participates in ensuring successful reproduction. Indeed, when day temperatures reach 35 °C (7 °C higher than standard greenhouse conditions), osmail1 mutants show increased sterility due to abnormal pistil development with about half of the plants developing three styles topped by stigmas.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Chemistry, Michigan State University, East Lansing, MI 48824.
The natural vibrational frequencies of biological particles such as viruses and bacteria encode critical information about their mechanical and biological states as they interact with their local environment and undergo structural evolution. However, detecting and tracking these vibrations within a biological context at the single particle level has remained elusive. In this study, we track the vibrational motions of single, unlabeled virus particles under ambient conditions using ultrafast spectroscopy.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706.
Given the influence of cognitive abilities on life outcomes, there is inherent value in identifying genes involved in controlling learning and memory. Further, cognitive dysfunction is a core feature of many neuropsychiatric disorders. Here, we use a combinatory in silico approach to identify human gene targets that will have an especially high likelihood of individually and directly impacting cognition.
View Article and Find Full Text PDFElife
January 2025
The University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, United Kingdom.
encodes three regulatory subunits of class IA phosphoinositide 3-kinase (PI3K), each associating with any of three catalytic subunits, namely p110α, p110β, or p110δ. Constitutional mutations cause diseases with a genotype-phenotype relationship not yet fully explained: heterozygous loss-of-function mutations cause SHORT syndrome, featuring insulin resistance and short stature attributed to reduced p110α function, while heterozygous activating mutations cause immunodeficiency, attributed to p110δ activation and known as APDS2. Surprisingly, APDS2 patients do not show features of p110α hyperactivation, but do commonly have SHORT syndrome-like features, suggesting p110α hypofunction.
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